Johnston S Claiborne, Easton J Donald
Department of Neurology, Box 0114, University of California at San Francisco, 505 Parnassus Ave, M-798, San Francisco, CA 94143-0114, USA.
Stroke. 2003 Oct;34(10):2446-50. doi: 10.1161/01.STR.0000090842.81076.68. Epub 2003 Sep 4.
Recent studies suggest that the short-term risk of stroke may be greater after transient ischemic attack (TIA) than after stroke.
We compared risks of neurological deterioration in those with and without TIA in the National Institute of Neurological Disorders and Stroke (NINDS) tissue plasminogen activator (tPA) trial, a randomized trial of intravenous tPA given within 3 hours of onset of cerebral ischemia, after excluding those with cerebral hemorrhage and those dying before 90 days of causes other than new ischemic stroke. TIA was defined as a National Institutes of Health Stroke Scale (NIHSS) score of zero at 24 hours. We chose subsequent deterioration as our outcome, defined as a worsening on the NIHSS at 90 days compared with 24 hours, so that episodes of new ischemia that may have been attributed to other causes would be included.
Of 498 subjects meeting entry criteria, 40 (8%) had TIA. Subsequent deterioration occurred in 30% of those with TIA and 10% of others (P=0.001, Fisher exact test). In multivariable models with adjustment for age, sex, ethnicity, 24-hour NIHSS score, tPA administration, presumed stroke subtype, and baseline systolic blood pressure, temperature, and glucose, TIA was an independent predictor of subsequent deterioration (odds ratio, 5.0; 95% CI, 2.0 to 12.5; P=0.001). Subsequent deterioration was not associated with tPA treatment, and there was no interaction between tPA administration, TIA, and subsequent deterioration. Lesser degrees of substantial acute recovery were also associated with greater risk of subsequent deterioration.
Patients with TIA may be a greater risk of subsequent neurological deterioration from causes other than hemorrhage. Substantial acute recovery may be an indicator of greater instability more broadly.
近期研究表明,短暂性脑缺血发作(TIA)后发生卒中的短期风险可能高于卒中后。
在国立神经疾病与卒中研究所(NINDS)组织型纤溶酶原激活剂(tPA)试验中,我们比较了有TIA和无TIA患者的神经功能恶化风险。该试验是一项随机试验,在脑缺血发作3小时内静脉给予tPA,排除了脑出血患者以及在90天内死于除新发缺血性卒中以外其他原因的患者。TIA定义为24小时时美国国立卫生研究院卒中量表(NIHSS)评分为零。我们选择随后的恶化作为结局指标,定义为90天时NIHSS评分较24小时时恶化,以便纳入可能归因于其他原因的新缺血发作。
在498名符合入选标准的受试者中,40名(8%)有TIA。有TIA的患者中30%发生了随后的恶化,其他患者中为10%(P=0.001,Fisher精确检验)。在对年龄、性别、种族、24小时NIHSS评分、tPA给药、推测的卒中亚型以及基线收缩压、体温和血糖进行调整的多变量模型中,TIA是随后恶化的独立预测因素(比值比,5.0;95%CI,2.0至12.5;P=0.001)。随后的恶化与tPA治疗无关,tPA给药、TIA与随后的恶化之间也没有相互作用。急性恢复程度较低也与随后恶化的风险较高相关。
TIA患者发生非出血性原因导致的随后神经功能恶化的风险可能更高。显著的急性恢复可能更广泛地表明更大的不稳定性。